Is there a role for an endothelium-derived relaxing factor in nociception?
Many of the circulating algesic agents released in response to ischemia produce a profound vasodilatation possibly through the release of an endothelium-derived relaxing factor (EDRF) as well as pain. We report here that intravenously administered S-nitrosocysteine, a putative EDRF, and not the nitric oxide liberating compound sodium nitroprusside produces significant alterations in nociceptive behavior that are abolished by bilateral vagotomy. These results are consistent with a role for EDRF in peripheral nociceptive mechanisms.
Meller
S T
ST
Department of Pharmacology, College of Medicine, University of Iowa, Iowa City 52242.
Lewis
S J
SJ
Bates
J N
JN
Brody
M J
MJ
Gebhart
G F
GF
D000704:Analysis of Variance; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003545:Cysteine / Q000031:analogs & derivatives* / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D009569:Nitric Oxide / Q000502:physiology*; D009599:Nitroprusside / Q000494:pharmacology; D010146:Pain / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D026403:S-Nitrosothiols; D014628:Vagotomy
D026403:S-Nitrosothiols; D009599:Nitroprusside; D009569:Nitric Oxide; C021315:S-nitrosocysteine; D003545:Cysteine